Mechanisms of heterosynaptic metaplasticity

Hulme, Sarah R., Jones, Owen D., Raymond, Clarke R., Sah, Pankaj and Abraham, Wickliffe C. (2014) Mechanisms of heterosynaptic metaplasticity. Philosophical Transactions of the Royal Society B: Biological Sciences, 369 1633: 1633.1-1633.8. doi:10.1098/rstb.2013.0148

Author Hulme, Sarah R.
Jones, Owen D.
Raymond, Clarke R.
Sah, Pankaj
Abraham, Wickliffe C.
Title Mechanisms of heterosynaptic metaplasticity
Journal name Philosophical Transactions of the Royal Society B: Biological Sciences   Check publisher's open access policy
ISSN 0962-8436
Publication date 2014-01-05
Year available 2013
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1098/rstb.2013.0148
Open Access Status DOI
Volume 369
Issue 1633
Start page 1633.1
End page 1633.8
Total pages 8
Place of publication London, United Kingdom
Publisher The Royal Society Publishing
Language eng
Subject 1100 Agricultural and Biological Sciences
1300 Biochemistry, Genetics and Molecular Biology
Abstract Synaptic plasticity is fundamental to the neural processes underlying learning and memory. Interestingly, synaptic plasticity itself can be dynamically regulated by prior activity, in a process termed 'metaplasticity', which can be expressed both homosynaptically and heterosynaptically. Here, we focus on heterosynaptic metaplasticity, particularly long-range interactions between synapses spread across dendritic compartments, and review evidence for intracellular versus intercellular signalling pathways leading to this effect. Of particular interest is our previously reported finding that priming stimulation in stratum oriens of area CA1 in the hippocampal slice heterosynaptically inhibits subsequent long-term potentiation and facilitates long-term depression in stratum radiatum. As we have excluded the most likely intracellular signalling pathways that might mediate this long-range heterosynaptic effect, we consider the hypothesis that intercellular communication may be critically involved. This hypothesis is supported by the finding that extracellular ATP hydrolysis, and activation of adenosine A2 receptors are required to induce the metaplastic state. Moreover, delivery of the priming stimulation in stratum oriens elicited astrocytic calcium responses in stratum radiatum. Both the astrocytic responses and the metaplasticity were blocked by gap junction inhibitors. Taken together, these findings support a novel intercellular communication system, possibly involving astrocytes, being required for this type of heterosynaptic metaplasticity.
Keyword Astrocytes
Gap junctions
Intercellular signalling
Long term depression
Long-term potentiation
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Queensland Brain Institute Publications
Official 2014 Collection
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Citation counts: TR Web of Science Citation Count  Cited 17 times in Thomson Reuters Web of Science Article | Citations
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